Four mechanisms leading to decreased cerebral perfusion and syncope—carotid hyperreactivity, left ventricular failure, arrhythmia, and left ventricular baroreceptor stimulation—were addressed by Richards et al. They studied four subjects with aortic stenosis (three with syncope, one with heart failure) using electrocardiographic and pressure monitoring of the pulmonary and brachial arteries. During bicycle exercise, a minimal increase in pressure occurred. However, during abrupt “climbing stairs at a sufficient pace to cause the onset of pre-syncopal symptoms,” they noted that even as the heart rate rose, there was an abrupt fall in both pulmonary and systolic arterial pressure associated with signs of tachypnea and pallor. No patients lost consciousness and all recovered within 60 seconds. However, there was only a gradual decrease in heart rate during the recovery period.
They emphasized that carotid sinus hyperreactivity was unlikely because of the absence of a sudden bradycardia with the fall in blood pressure. Secondly, they noted no arrhythmias. Thirdly, they ruled out the possibility of left ventricular failure because pulmonary arterial pressures did not rise. They felt that the left ventricular baroreceptor response best explained this phenomenon and attributed a lack of bradycardia, as observed in animals, to species differences. They suggested that the absence of hypotension with bicycle exercise was due to the gradual stepwise incremental exercise versus the sudden onset of strenuous exertion in stair climbing necessary for the receptor response.
In our patient, there was a blunted blood pressure response followed by a 10 mm drop in systolic pressure after the first stage of exercise. After initially developing sinus tachycardia, he developed atrial and ventricular dysrhythmias immediately followed by a profound bradycardia. These are consistent with left ventricular baroreceptor stimulation during exertion. However, other mechanisms cannot be excluded. For example, the patients marked ST segment depression along with a blunted blood pressure response suggests myocardial ischemia with consequent left ventricular dysfunction and reduced cardiac output. Although the patient had normal coronary arteries by angiography, it has been demonstrated, using Doppler flow probes, that with ventricular hypertrophy, there is decreased coronary reserve. This has been hypothesized to be an important contributor to angina pectoris in patients with normal coronary arteries and aortic stenosis. Subendocardial ischemia has also caused arrhythmias in patients with marked left ventricular hypertrophy and may explain the ventricular arrhythmias, and acute left atrial dilation may be a source for atrial arrhythmias.